Abstract
Hypertension is associated with cognitive deficits. Angiotensin converting enzyme inhibitors (ACEI) improve cognitive decline in hypertensive patients. We hypothesized that centrally active ACEI captopril (CTP) would alleviate cognitive function by improving endothelium dependent dilation and middle cerebral artery (MCA) remodeling from stroke prone spontaneously hypertensive rats (SHRSP). Data are shown as mean±SEM, SHRSP vs CTP and are analyzed by Student’s t‐test. 12 week old male SHRSP received CTP (50 mg/kg/day) for 6 weeks. Cognitive function, evaluated by Morris water maze, showed no difference between groups. CTP reduced systolic blood pressure (178±8 vs 131±6 mmHg, p<0.05). MCA reactivity and passive structure was assessed by pressure myography (data shown at 80 mmHg). CTP did not increase lumen diameter (232.6±8.1 vs 249.1±8.1). CTP reduced wall thickness (21.9±0.1 vs 17.3±1.0 µm, p<0.05) and wall/lumen ratio (0.1±0.01 vs 0.07±0.01, p<0.05). CTP improved endothelial function as evidenced by enhanced dilation to 10 µM adenosine diphosphate (change in diameter from baseline at: 36.2±1.0 vs 54.2± 5.3 µm, p<0.05). CTP increased resting pial artery perfusion (673±32 vs 750±201 laser Doppler units, p<0.05). These data suggests that while CTP does not affect cognitive abilities, it may contribute to increased baseline perfusion by enhancing dilation and reversing remodeling of MCAs.
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